The use of antibacterial agents has become a mainstay in healthcare in the 21st century. Since the work of Pasteur and Koch to link a role of bacterial pathogens to disease, we as a society have been driven to develop chemotherapeutics to prevent transmission and to cure microbiological related disease. In recent years, over- and mis-use of these drugs has led to the emergence of resistant pathogens.
Resistance of a bacterium to antibiotics can arise through various mechanisms including modulation of intracellular concentration of the drug through efflux pumps, hindrance of drug influx (e.g. through biofilm formation), enzymatic inactivation, or through modification of the target of the drug.1,2 Very few classes of antimicrobials have been marketed in the past 46 years (oxazolidinones3 and lipopeptides4). At this pace drug research and discovery may not be able to maintain the tenuous hold that we have on infectious disease. This is particularly evident in the emergence of multi-drug resistant pathogens “superbugs” where health care workers are left with few options for treatment.5 The Gram-positive Staphylococcal, Streptococcocal, Enterococcal, and now Clostridium pathogens have proven to be a particular challenge in this respect.6,7 
In small molecule antimicrobial design, the current methods of drug discovery aim to exploit cellular differences between bacterial and human biology to prevent host toxicity from the developed drug. This methodology however limits the effective number of targets that can be exploited for drug design to a few cellular processes. These processes typically include bacterial cell wall biosynthesis, DNA synthesis and protein synthesis, which have been mined considerably for the development of antibiotics since the mid 1940s.